Evidence map›Paper›PMID 20061370›Full record

ArticleNucleic acids research2010

A truncated DNA-damage-signaling response is activated after DSB formation in the G1 phase of Saccharomyces cerevisiae.

Ryan Janke, Kristina Herzberg, Michael Rolfsmeier, Jordan Mar, Vladimir I Bashkirov, Edwin Haghnazari, Greg Cantin, John R Yates, Wolf-Dietrich Heyer

Open access · goldAbstract read
In one paragraph

Article in Nucleic acids research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.6field-weighted citation impact, top 17% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

16 citing papers in PubMed, 26 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Article
  6. Rad52 phosphorylation by Ipl1 and Mps1 contributes to Mps1 kinetochore localization and spindle assembly checkpoint regulation.Proceedings of the National Academy of Sciences of the United States of America · 2017
    Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors at 2 institutions in 1 country.

Ryan JankeDepartment of Microbiology, University of California, Davis, CA 95616-8665, USA.
Kristina Herzberg
Michael Rolfsmeier
Jordan Mar
Vladimir I Bashkirov
Edwin Haghnazari
Greg Cantin
John R Yates
Wolf-Dietrich Heyer
University of California, Davis · USScripps Research Institute · US

Funding

ZDS2P REGULATES SWE1P-DEPENDENT POLARIZED CELL GROWTH IN S CEREVISIAEP41RR011823 · NCRR · UNIVERSITY OF WASHINGTON · PI DAVIS, TRACY · 1996 to 2011
$24.7M
ENVIRONMENTAL TOXICOLOGYT32ES007059 · NIEHS · UNIVERSITY OF CALIFORNIA DAVIS · PI Laura S Van Winkle · 1985 to 2026
$7.9M
Regulation of Recombinational DNA RepairR01CA092276 · NCI · UNIVERSITY OF CALIFORNIA DAVIS · PI HEYER, WOLF-DIETRICH · 2001 to 2020
$5.2M
NCI NIH HHS R01 CA092276NCI NIH HHS R01 CA92276NCRR NIH HHS P41 RR011823NIEHS NIH HHS T32ES007059
6 · The paper itself

Abstract

In Saccharomyces cerevisiae, the DNA damage response (DDR) is activated by the spatio-temporal colocalization of Mec1-Ddc2 kinase and the 9-1-1 clamp. In the absence of direct means to monitor Mec1 kinase activation in vivo, activation of the checkpoint kinase Rad53 has been taken as a proxy for DDR activation. Here, we identify serine 378 of the Rad55 recombination protein as a direct target site of Mec1. Rad55-S378 phosphorylation leads to an electrophoretic mobility shift of the protein and acts as a sentinel for Mec1 activation in vivo. A single double-stranded break (DSB) in G1-arrested cells causes phosphorylation of Rad55-S378, indicating activation of Mec1 kinase. However, Rad53 kinase is not detectably activated under these conditions. This response required Mec1-Ddc2 and loading of the 9-1-1 clamp by Rad24-RFC, but not Rad9 or Mrc1. In addition to Rad55-S378, two additional direct Mec1 kinase targets are phosphorylated, the middle subunit of the ssDNA-binding protein RPA, RPA2 and histone H2A (H2AX). These data suggest the existence of a truncated signaling pathway in response to a single DSB in G1-arrested cells that activates Mec1 without eliciting a full DDR involving the entire signaling pathway including the effector kinases.

Indexed as

DNA Breaks, Double-StrandedG1 PhaseSignal TransductionAdaptor Proteins, Signal TransducingCell Cycle ProteinsCheckpoint Kinase 2DNA-Binding ProteinsDNA RepairElectrophoretic Mobility Shift AssayHistonesIntracellular Signaling Peptides and ProteinsPhosphorylationProtein Serine-Threonine KinasesSaccharomyces cerevisiaeSaccharomyces cerevisiae ProteinsSerineAdaptor Proteins, Signal TransducingCell Cycle ProteinsCheckpoint Kinase 2DNA-Binding ProteinsHistonesIntracellular Signaling Peptides and ProteinsLCD1 protein, S cerevisiaeMEC1 protein, S cerevisiaeProtein Serine-Threonine KinasesRAD53 protein, S cerevisiaeRAD55 protein, S cerevisiaeRPA2 protein, S cerevisiaeSaccharomyces cerevisiae ProteinsSerine

Identifiers

PMID20061370
PMCPMC2853130
OpenAlexW2153560282

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.